The objective of this sutdy is to investigate the role of systemic arterial reflexes and local mechanical factors in the pulmonary vascular response to atelectasis or alveolar hypoxia in the conscious, spontaneously breathing dog. We have demonstrated that the reduction in blood flow to an acutely hypoxic lung depends upon system PO2 in conscious, spontaneously breathing dogs. If systemic arterial PO2 is kept at or above normal levels, then blood flow to the hypoxic lung decreases. Stimulation of the systemic arterial chemoreceptors with hypoxemia or cyanide interferes with this response. After a control period of bilateral l00% O2, dogs with electromagnetic flow probes chronically implanted on their left and main pulmonary arteries and breathing through Carlens dual-lumen endotracheal tubes are either subjected to left lung atelectasis or l00% N2 ventilation of the left lung. Redistribution of pulmonary blood flow away from unilaterally hypoxic or atelectatic lung is assessed by the change in the ratio of left pulmonary artery blood flow to main pulmonary artery blood flow. Systemic reflexes will be stimulated by administering room air to the "normoxic" lung to lower PaO2 or NaCN injection (chemoreflex), or removal of moderate amounts of blood (baroreflex). Experiments will be repeated after adrenergic blockade, with constant or elevated PACO2 and after sinoaortic denervation. The effects of changes in cardiac output on the hypoxic pulmonary vasoconstriction will be tested in two ways. Cardiac output can be increased during normoxemic unilateral atelectasis or hypoxia by blood transfusion. The increase in cardiac output that occurs during unilateral atelectasis or hypoxia with hypoxemia will be prevented by inflating a balloon inside the inferior vena cava while cardiac output is monitored. The data obtained should contribute to our understanding of the control of pulmonary blood flow and the maintenance of ventilation-perfusion relationships and may be of great value in interpreting the mechanisms involved in the Adult Respiratory Distress Syndrome.